Multiple sclerosis is a chronic disease characterized by recurrent attacks of neurologyc dysfunction, due to lesions in the whate matter of the center nervous system. MS lesions evolve over time. "Active" lesions contain inflammatory cells such as lumphocytes, plasma cells, and macrophages in areas of demyelination, with evidence of phagocytosis of myelin and its breakdown products by macrophages. In contrast "inactive" lesions are hypocellular with scarring and loss of oligodendrocytes, the cells that produce myein. The presence of leukobytes in the CNS, where thay are normally absent, together with their early association with the demyelinating process, suggests that inflammation is involved in the pathogenesis of MS. Although the cause of MS is unknown, data from the published literature support immunologic or infectious factors leading to the state of chronic CNS inflammation. Migration of lymphocytes across the blood brain barrier and development of CNS inflammation is a hallmark of acute symptoms of multiple sclerosis. We will test the hypotheses that agents which interfere with the migration of cell by preventing adhesion of lymphocytes to capillary endothelium of the brain, will retard the inflammatory process and reduce or prevent the development of neurologic symptoms.